Parkinson's Disease Medical Guide (Introduction)
What is Parkinson's?
Parkinson’s disease (PD), also known as "shaking palsy," or Parkinsonism, mostly affects individuals over the age of 60. It primarily manifests as slow movement, tremors in hands, feet, or other parts of the body, and a loss of flexibility, leading to stiffness. The British physician James Parkinson first systematically described the condition, initially naming it "shaking palsy" due to the lack of understanding about its classification at the time. Parkinson's disease is the fourth most common neurodegenerative disorder among the elderly, affecting 1% of individuals aged 65 and 0.4% of those over 40. The disease can also occur in children and adolescents. Between 50% to 80% of cases develop insidiously, with the initial symptom often being a 4-8 Hz resting "pill-rolling" tremor in one hand. Speech disorders are common among patients with Parkinson's.
What are the symptoms of Parkinson's? Are there any special symptoms? What are the early symptoms of Parkinson's?
Clinical Manifestations
Parkinson’s disease usually develops between the ages of 40 and 70, with an increased incidence after 60. Onset before the age of 30 is rare. In a group of 380 PD patients, only four cases were reported. Males are slightly more affected. The onset is subtle and progresses slowly, mainly manifesting as resting tremors, increased muscle tone, and bradykinesia. The order of symptom appearance varies from person to person. Tremors are the first symptom in 60%-70% of cases, followed by gait disturbances (12%), muscle rigidity (10%), and bradykinesia (10%). Symptoms typically start in one upper limb and gradually spread to the same-side lower limb, opposite upper limb, and lower limb, following an "N"-shaped progression (65%-70%). In 25%-30% of cases, symptoms begin in one lower limb, with simultaneous bilateral lower limb involvement being extremely rare. Many cases still exhibit left-right differences in symptoms even in late stages.
Regardless of treatment, the chronic progressive course and the need for assistance within a few years are inherent clinical characteristics. Diagnosis is generally clear based on typical PD manifestations and positive responses to dopaminergic drugs. However, recognizing certain subclinical symptoms or atypical cases in the early stages remains challenging, significantly impacting quality of life later on. This is currently a research focus in clinical neuroscience. For most patients and clinicians, it is difficult to definitively determine the onset date, initial symptoms, and timing of slowness or tremor symptoms. According to domestic reports by Li Dianian et al., preclinical symptoms may last 3-5 years, dividing PD symptoms into preclinical and clinical phases.
1. Preclinical Symptoms
The earliest mention of preclinical symptoms was by Fletcher (1973) et al., but these symptoms have yet to gain widespread attention. These symptoms mainly include:
(1) Sensory abnormalities: As early as in Parkinson's "Shaking Palsy," it was noted that "some PD cases experience rheumatoid-like pain before motor symptoms appear." Charcot similarly described two PD patients the same year. In the 1970s, Fletcher and Snider provided detailed descriptions of PD preclinical symptoms and sensory disorders. In the 1980s, William classified sensory disorders using electrophysiology, reporting symptoms like numbness, tingling, crawling sensations, and burning in affected limbs' joints, particularly wrists and ankles. Initially intermittent or migratory, they become fixed later. Routine neurological exams reveal no significant objective sensory abnormalities, but electrophysiological tests show prolonged latency and conduction times in somatosensory evoked potentials (SEPs), especially in the lower limbs. By the early 1990s, our retrospective survey of 150 patients showed all experienced varying degrees of sensory abnormalities in affected limbs before clinical symptoms appeared, which could persist continuously but not parallel to motor impairments. Electrophysiological tests revealed cortical delays and prolonged latencies in somatosensory and cortical evoked potentials.
(2) Restless limbs and fatigue: Besides subjective sensory abnormalities, approximately half of patients experience indescribable discomfort in affected limbs, such as soreness, swelling, numbness, or pain, especially during rest after exertion. These symptoms alleviate with tapping or massaging, resembling restless leg syndrome. Some patients experience easy fatigue in affected limbs, particularly in wrist, shoulder, ankle, and knee joints, where slight tremors may occur after exertion. Initial use of general analgesics may be effective, but this diminishes after a few months. Dopaminergic drugs can then produce significant effects.
2. Clinical Phase Symptoms
Initial symptoms vary greatly among individuals. Reports indicate subjective sensory abnormalities in 85%, tremors in 70.5%, rigidity or bradykinesia in 19.7%, clumsiness or writing difficulties in 12.6%, gait disturbances in 11.5%, myalgia/spasms/pain in 8.2%, psychiatric symptoms like depression/anxiety in 4.4%, speech disorders in 3.8%, generalized weakness/muscle weakness in 2.7%, drooling and masked face each in 1.6%.
(1) Resting Tremor: Often the first symptom of PD, though some patients, especially those over 70, may not exhibit tremors. The mechanism involves irregular, alternating activity of affected muscles and antagonistic muscles. Early signs include distal limb involvement, starting unilaterally, commonly in the hand. Some cases start in the knee. When rotational components are involved, thumb and index finger may exhibit pill-rolling tremors. Tremor frequency is generally 4-8 Hz, appearing at rest, stopping with strong movements, worsening with tension, and disappearing during sleep. Over several years, tremors may involve contralateral limbs or sides, and severe cases may affect the head, jaw, lips, tongue, throat, and all limbs. Asking patients to move one limb, such as clenching or unclenching a fist, may induce tremors in the opposite limb, aiding in detecting early mild tremors. Later, some patients may experience action or postural tremors alongside resting tremors.
(2) Rigidity: A major symptom of PD, caused by increased tension in agonist and antagonist muscles. If present throughout passive movement, it is termed "lead-pipe rigidity," and if combined with tremors, "cogwheel rigidity." Early rigidity occurs in the wrist and ankle of the affected side, especially after exertion, with gear-like muscle tension felt during gentle passive movement. Increased muscle tension leads to various abnormal symptoms, such as reduced blinking, chewing, swallowing, and walking.
Clinical trials helpful in detecting mild rigidity include: ① Asking patients to move the opposite limb, making rigidity in the examined limb more evident; ② Head Dropping Test: When lying supine, quickly removing the pillow under the head causes the head to fall slowly rather than rapidly; ③ Placing both elbows on a table with forearms perpendicular to it, relaxing arm and wrist muscles. Normally, the wrist forms a 90-degree angle with the forearm, whereas PD patients maintain varying degrees of wrist extension, resembling upright road signs, known as the "road sign phenomenon." Muscle rigidity causing joint pain in elderly patients results from increased muscle tension obstructing joint blood supply.
(3) Bradykinesia: Manifested as reduced voluntary movements, including difficulty initiating and slow movement, due to increased muscle tone and impaired posture reflexes. Symptoms include delayed movements when getting up, turning over, walking, and changing directions, reduced facial expression, eye fixation, reduced blinking forming a masked face, difficulty with fine finger movements like buttoning clothes or tying shoelaces, and progressively smaller handwriting, known as micrographia.
Bradykinesia is the main cause of disability in PD patients. Previously thought to result from rigidity, it is now understood to be unrelated. Evidence suggests that reduced or absent movement in PD is complex, related to dysfunction in subcortical extrapyramidal drive mechanisms or descending extrapyramidal motor activation systems. Surgical treatment improves rigidity but does not consistently enhance movement frequency like dopaminergic drugs.
(4) Posture and Gait Abnormalities: Impaired posture reflexes are the primary symptoms causing difficulties in daily living, second only to reduced or absent movement. Patients exhibit a unique flexed posture with neck and trunk rigidity, head forward inclination, elbow flexion, wrist extension, forearm pronation, interphalangeal joint extension, thumb opposition, hip and knee flexion. Early dragging of legs progresses to small steps, difficulty starting, rushing forward after starting, accelerating, and inability to stop or turn promptly, known as festination. Reduced or absent arm swing occurs while walking, and turning involves stiff trunk movements due to balance issues. Patients fear falling and hesitate at obstacles. As the disease progresses, posture impairments worsen, and standing up from sitting or lying becomes difficult in advanced stages. The exact mechanism of posture reflex impairment in PD patients remains unclear, possibly linked to damage in the pallido-thalamo-cortical output loop.
(5) Other Symptoms:
① Repeatedly tapping the patient's supraorbital margin can induce persistent blinking (Myerson's sign), unlike normal reactions.
② Dysfunctions in mouth, pharynx, and palate muscles lead to slow speech, low-pitched monotonous voices, drooling, and severe swallowing difficulties.
③ Hypersecretion in sebaceous and sweat glands causes oily faces and excessive sweating, gastrointestinal motility disorders cause stubborn constipation, and autonomic nervous system dysfunctions lead to orthostatic hypotension without sphincter involvement.
④ Psychiatric symptoms include depression, anxiety, agitation, and mild cognitive decline or visual hallucinations in some late-stage patients, usually not severe.
3. Clinical Classification and Typing of PD
Written by Wang Xin-de, established at the October 1984 National Extrapyramidal System Conference.
(1) Primary (Idiopathic Parkinson's Disease, i.e., Shaking Palsy):
① Based on disease course:
A. Benign type: Longer course, averaging 12 years. Motor symptom fluctuations and psychiatric symptoms appear later.
B. Malignant type: Shorter course, averaging 4 years. Motor symptom fluctuations and psychiatric symptoms appear earlier.
② Based on symptoms:
A. Tremor type.
B. Hypokinesia and rigidity type.
C. Tremor-hypokinesia-rigidity-dementia type.
D. Tremor-hypokinesia-rigidity-non-dementia type.
③ Based on genetics:
A. Familial Parkinson's Disease.
B. Juvenile Parkinson's Disease.
(2) Secondary (Parkinsonism, Symptomatic Parkinsonism):
① Infectious (including chronic viral infections): Postencephalitic Parkinsonism (sleeping sickness encephalitis, other encephalitides).
② Toxic (carbon monoxide, manganese, carbon disulfide, hydrocarbons, methanol, etc.).
③ Drug-induced (antipsychotic drugs like phenothiazines, butyrophenones, reserpine, and levodopa, etc.).
④ Cerebrovascular lesions.
⑤ Brain tumors (especially midline brain tumors).
⑥ Brain trauma.
⑦ Midbrain cavitation.
⑧ Metabolic (hypothyroidism, basal ganglia calcification, chronic hepatic encephalopathy, etc.).
(3) Symptomatic Parkinsonism (Heterogeneous System Degeneration):
① Progressive Supranuclear Palsy.
② Striatonigral Degeneration.
③ Corticobasal Ganglionic Degeneration.
④ Olivopontocerebellar Atrophy.
⑤ Shy-Drager Syndrome (Orthostatic Hypotension).
⑥ Dementia [Guam Parkinson-Dementia-Amyotrophic Lateral Sclerosis Syndrome, Jacob-Creutzfeldt Disease (Corticostriatal Spinal Degeneration), Alzheimer's and Pick's Diseases, Normal Pressure Hydrocephalus].
⑦ Genetic Diseases (Wilson's Disease, Hallervorden-Spatz Disease, Huntington's Disease, Spinocerebellar Nigral Degeneration, etc.).
Diagnosis
1. Diagnostic Criteria
(1) Onset in middle-aged or elderly individuals, with a slow progressive course.
(2) At least two of the four main signs (resting tremor, rigidity, bradykinesia, posture/gait disturbance), with at least one of the first two, and asymmetrical symptoms.
(3) Levodopa treatment is effective, with positive levodopa or apomorphine tests supporting a primary PD diagnosis.
(4) No extraocular muscle paralysis, cerebellar signs, positional hypotension, pyramidal tract damage, or muscle atrophy. Clinical diagnosis of PD correlates with autopsy pathology findings in 75%-80% of cases.
2. Common Diagnostic and Differential Diagnostic Standards Domestically and Internationally
(1) Diagnosis of Idiopathic Parkinson's Disease (IPD): Established by Wang Xin-de at the October 1984 National Extrapyramidal System Conference:
① At least two of the four typical symptoms and signs (resting tremor, bradykinesia, rigidity, position reflex disorder).
② Absence of atypical symptoms and signs inconsistent with IPD diagnosis, such as pyramidal tract signs, apraxic gait disorders, cerebellar symptoms, intention tremor, gaze palsy, severe autonomic dysfunction, and prominent dementia with mild extrapyramidal symptoms.
③ Decreased homovanillic acid in cerebrospinal fluid helps confirm early Parkinson's Disease (PD) and differentiate it from Essential Tremor (ET) and drug-induced Parkinsonism.
Generally speaking, ET is sometimes hard to distinguish from early IPD, with ET showing positional and action tremors in hands and head without increased muscle tone or bradykinesia.
(2) Diagnosis of Secondary Parkinsonism (SPDS):
① Drug-induced PS (MPS): Clinically similar to IPD, relying on history of antipsychotic drug use for differentiation. MPS symptoms are usually symmetrical, sometimes accompanied by hyperactivity on one side. If clinically difficult to distinguish, discontinuing antipsychotics temporarily can help, as MPS symptoms generally disappear within weeks to six months.
② Vascular PS (VPS): Characterized by absence of tremor, often with focal neurological signs (pyramidal tract signs, pseudobulbar palsy, emotional instability), stepwise progression, and generally ineffective L-dopa treatment.
(3) Diagnosis of Symptomatic Parkinsonism Syndrome (Heterogeneous System Degeneration):
① Progressive Supranuclear Palsy: Sometimes hard to differentiate from Parkinson's. Key features include reduced movements, neck rigidity with backward tilt, pseudobulbar palsy, and upward gaze palsy.
② Olivopontocerebellar Atrophy: Needs differentiation from primary Parkinson's. Clinically, it can present with bradykinesia, rigidity, and even resting tremor, but often with cerebellar ataxia. CT shows characteristic changes. Blood glutamate decarboxylase activity is reduced.
③ Striatonigral Degeneration: Very similar to primary Parkinson's, clinically difficult to differentiate, mainly relying on pathological diagnosis. If L-dopa treatment is ineffective, striatonigral degeneration should be considered.
④ Shy-Drager Orthostatic Hypotension Syndrome: Presents with orthostatic hypotension, urinary and fecal incontinence, anhidrosis, distal muscle atrophy in limbs. Sometimes associated with Parkinsonism. If patients exhibit Parkinsonism and mild autonomic dysfunction, differentiation from primary Parkinson's is necessary.
⑤ Dementia: Dementia accompanied by Parkinsonism is not uncommon. Alzheimer's disease: Late-stage Alzheimer's presents with dementia along with extrapyramidal symptoms...
[Reference Link](http://www.mingyihui.net/article_389.html)